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Muscles

Muscles. Striated Cardiac Smooth Excitability and contractibility. animations. http://www.dnatube.com/video/4875/Physiology-of-muscle-contraction-and-relaxation http://www.dnatube.com/video/1306/Role-of-myosin-crossbridge-in-the-contraction-of-muscle

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Muscles

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  1. Muscles Striated Cardiac Smooth Excitability and contractibility

  2. animations • http://www.dnatube.com/video/4875/Physiology-of-muscle-contraction-and-relaxation • http://www.dnatube.com/video/1306/Role-of-myosin-crossbridge-in-the-contraction-of-muscle • http://www.dnatube.com/video/1952/Sliding-filament-causes-contraction-of-muscle • http://www.dnatube.com/video/4154/Cellular-mechanism-of-muscular-contraction

  3. Striated muscle – sarcomere

  4. Striated muscle – sliding of contractile elements

  5. Striated muscle – motor unit

  6. Striated muscle – neuromuscular junction

  7. Striated muscle – myography, tetanus • Muscle contraction • Twitch • Summation • Superposition • Tetanus • Smooth - multiple summation • Undulating – multiple superposition

  8. Muscle strength • Muscle strength depends on the number of motor units recruited • Strength dependsonly on cross-sectional area20 – 100 N per sq.cmMuscle cells cannot divide. Thickening is formed by duplication of myofibrils. • Muscle strenght is influenced • genetically • hormonally – testosterone, anabolics

  9. Muscle strength – tension/length curve, isometric and isotonic contraction

  10. Sources of energy for muscle contraction • ATP – maintains contraction for 1 to 2 seconds • phosphocreatine – 5 times as great as ATP, sufficient for7-8 scontraction • Anaerobic Glycolysis • Enzymatic breakdown of the glucose to pyruvate and lactate liberates energy that is used to convert ADP to ATP, glycolysis can sustain contraction for about 1 min • Twofold importance of glycolysis • Reactions occurs in the absence of oxygen(muscle contraction can be sustained for a short time when oxygen is not available) • The rate of formation of ATP is2.5 times as rapid as ATP formation with oxygen • Oxidative metabolism– the final source of energy • 95% of all energy used by the muscle

  11. Function of ATP ATP is necessary for • Muscle contraction – detachment of the head of myosin from the actin • Function of Na+/K+pump • Function of Ca++pump Physiological depletion of sources of ATP (reversible) – contracture, spasm, cramp Irreversible loss of all ATP – rigor mortis • Lack of energy for the separation of cross-bridges • Rigor is faster after muscle fatigue and exhaustion • Muscles remain in rigor until muscle proteins are destroyed by autolysis (15-25 hours)

  12. Muscle fatigue • Acute (recovery - within 24 hours) and chronic (may be followed by a complete exhaustion) • Decrease force of muscle contraction • Fatigue • in the neuromuscular junction • Accumulation of extracellular K+ may lead to a disturbance in depolarization, reduction of the amplitude of the action potential and conduction velocity • decreasing amounts of muscle glycogen • Accumulation oflactate – lower pH, increase of K+, stimulation of the free nervous endings – pain, edemas • exhaustion of ATP

  13. Striated muscle – twitch = types of muscles

  14. Muscle pain • After exercise • Dull ache when moving or being palpated • Begins in 1-3 days and lasts for one week • Maximal isometric strength is not impaired • Does not correlate with muscle edema, plasma CK, inflammation markers During exercise • Ischemic, hypoxic, accumulation of metabolites, pH • Fast in, fast out • Difficult to localize (muscle, bone, tendom, joint) • Referred pain (viscero somatic hyperalgesia)

  15. Botulinum toxin preventsacetylcholine release– spasms (torticolis) Methacholine, carbachol and nicotine – the same effect as Ach – not destroyed by acetylcholinesterase – long action – Ophtalmology (glaucoma) Muscle relaxants– general anesthesia – muscle relaxation. Curare (D-tubocurarine) blocks acetylcholine receptorsw/o depolSuccinylcholine is a depolarizing blocker Anticholinesterase drugs, neostigmine and physostigmine– reversible inactivation of acetylcholinesterase – accumulaiton of Ach – myasthenia gravis Organophosphate – chemical weapons – irreversibleinactivation ofacetylcholinesterase– cramps, respiratory distress, sweating and convulsions. Dandrolen blocks Ca realease from SR – malignant hypetermia Drugs that modify neuromuscular junction

  16. Smooth muscle - structure actin and myosin no troponin, calmodulin instead Dense bodies – analog of Z-lines – attachment of actin filaments Actin – long filaments, 15 times as myosin • Contraction 30 times slower than that of sceletal muscle • constant power during contraction (isotonic line longer,since some contractile units have optimal overlapping of A&M at one length of the muscle and others at other length)

  17. Types of smooth muscles • Multiunite • discrete smooth muscle • single nerve ending • The ciliary muscle of the eye(parasympathetic control) • The piloerector muscles(sympathetic control) • Single-unit (visceral) • Hundreds to millions contract together– syncythial • gap junction – ions can flow freely • gut, bile ducts, ureters, uterus, vessels

  18. Contraction of smooth muscle • Initiating event in smooth muscle contraction is an increase in intracelullar Ca2+ ions cause by: • Nerve stimulation • Stretch of the fiber • Hormonal stimulation • Changes in the chemical environment of the fiber • Strength of contraction depends on extracellular Ca2+ • Removal of Ca2+ ions is achieved by calcium pump, calcium pump is much slower in comparison with a pump of skeletal muscle – longer contraction

  19. Mechanism of contraction • Beginning of contraction 4 Ca2+ bind with regulatory proteincalmodulin Complex Ca-calmodulin activatesenzyme myosin kinase (a phosphorylating enzyme) Light chain of of each myosin head (regulatory chain) become phosphorylated, the head has the capability of binding with the actin filaments • Cessation of contraction: When the concentration of Ca2+ falls bellow a critical level, all processes automatically reverse except for thephosphorylation of myosin head Enzymemyosin phosphatase splits the phosphate from the regulatory light chain

  20. Smooth muscle - contraction

  21. Smooth muscle – membrane potential • Resting potential –50 to –60 mV • Spontaneous slow wave (some smooth muscle is self-excitatory) • Slow wave can initiate action potentials (-35 mV) • The more AP, the stronger contraction Slow wave Smooth muscle has more voltage-gated calcium channels and very few voltage-gated sodium channels than skeletal m. Importance of Ca2+ ions in generating smooth muscle action potential – phase plateau of AP, contraction

  22. Contraction without action potentials • In multiunite smooth muscle, Ca2+ions can flow into the cellthrough the ligand-gated Ca2+channel • ligand – acetylcholine, norepinephrine • Action potentials most often do not develop • Membrane potential do not reach a critical levelfor generating action potential because the Na+pump pumps sodium ions out of the cell

  23. Regulation of smooth muscle Smooth muscle are regulated by autonomic nerves Nerve fibers do not make direct contact with smooth muscle fibers – they formed so-called diffuse junction Terminal axons have multiple varicosities, containing vesicules In the multiunite type of smooth cells, the contact junctions are similar to the end plate of skeletal muscle

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